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We first note that the variation in the final position of the juvenile cells in the ventral cord provides a natural explanation for the observed variation in the order of cell classes (White et al. 1975). Furthermore, the periodicity in ancestry of the late cells corresponds very well to the periodicity in five of the cell classes. If we suppose that there is a one-to-one correspondence between the ancestry of a late cell and its class, we find that only one self-consistent set of allocations can be made within the observed limits of variation (table 3).
The reason for comparing the lineage data with previously established electron microscopic assignments is that sectioning the ventral cord and tracing neuronal connections is extremely time-consuming. It is therefore impracticable to test the proposed allocations exhaustively. However, the expected relationships were confirmed directly for a short stretch of ventral cord in one animal (table 4).
The non-linear arrangement of cells in the r.v.g. precludes comparison with known assignments. The lineage of the late cells in two r.v.gs was therefore determined and the cells were identified by serial section electron microscopy. The allocations are identical for the two r.v.gs, but differ in the case of three cells from those for the ventral cord (table 5).
The failure of P1a to become a VA cell draws a distinction between precursors P1 and P2, which were symmetrically arranged in the young L1. In the male there is an additional difference between them in that P1c dies but P2c survives. This may mean that P1 is already determined before migrating into the ventral cord and that it is thereby constrained to enter the cord anterior to P2. Alternatively, the fates of cells may be partly determined by local influences.
An interesting feature of the allocations given in table 3 is that in the adult the axons of the juvenile cells innervate solely the dorsal cord. It seems unlikely that the L1 entirely lacks ventral innervation, and indeed White has shown (unpublished observations) that in the young L1 the DD cells innervate the ventral cord instead of the dorsal cord. The events at the L1 moult, therefore, include the loss of old neuronal connections as well as the addition of new ones.
It appears then, that the pattern of division shown in figure 2 partially determines the function of the cells to which it gives rise. There are two extreme ways in which this could occur. First, a distinction may be made between the anterior and posterior daughter at each division, and this information may be accumulated to determine the properties of the differentiated cells. Secondly, the position of a cell in the final array may be the determining factor. It is hoped eventually to distinguish between these possibilities by selective destruction of cells during the division process. For the present, the following observations tend to support the first mechanism.
(1) The division pattern itself requires anterior and posterior daughters to be distinguished in some way.
(2) The variable movement of the dividing nuclei among the juvenile nuclei suggests that specific cytoplasmic bridges between the late cells would be required for the second mechanism. However, the death of a c cell frequently precedes the generation of the corresponding a and b cells, indicating that at least the a/b determination is independent of contact with the other cells.
If, indeed, there is lineal determination of cell function, the phenomenon of programmed cell death takes on particular significance. For, if each precursor is committed to producing a fixed array of five cell types, the destruction of a cell whose function is not required at a given location is entirely reasonable. Mechanisms of this sort provide a possible explanation for the widespread occurrence of 'histogenetic' cell death in embryogenesis (Saunders 1966).
The pattern of c cell death is just one aspect of the different roles played by these neurones in the two sexes. White et al. (1976) have shown that, in the hermaphrodite, VC cells make relatively few synapses with the body muscles but form an important input to the muscles of the vulva; in the male, on the other hand, the far more numerous VC cells have no vulva to innervate. A possible interpretation of these observations is that in the male the VC neurons are excitatory to the body muscles, being responsible for the characteristic arching reflex; in the hermaphrodite this function is not required, but some of the VCs are retained and employed in control of the vulva. Such sexual re-allocation parallels the positional re-allocation seen in the r.v.g.
In a general way, it is also possible to explain the loss of a VA cell anteriorly and a VB cell posteriorly. Since the axons of VA cells project forwards to the next most anterior set of muscle synapses, and those of VB cells project backwards (White et al. 1976), end effects of some kind are inevitable. We may therefore regard the re-allocation of an a cell in the r.v.g. and the death of a b cell in the p.a.g. as equivalent events. It is not clear, though, why two cells should be affected at each end, especially in view of the re-allocation of Pod as a VA in the r.v.g. It will be interesting to see whether P12d or P12e is re-allocated as a VB in the p.a.g.
FIGURE 8S- 14. Photographs of larvae in Nomarski interference contrast. Lateral aspect, magn. x 2000. The
small bright objects within the nematode are storage granules in the gut and elsewhere. In some pictures
bacteria are adhering to the cuticle of the nematode. Types of nuclei: J, juvenile nerve; P, precursor; f,
ventral hypodermal; gu., gut; go., gonad; h., lateral hypodermal; mu., muscle.
FIGURE 8. L1, before precursor migration.
FIGURE 9. L1, after precursor migration.
FIGURE 10. L1, during ventral cord development. The arrow points to a metaphase nucleus.
FIGURE 11. L2, showing nerve and hypodermal nuclei in the mature ventral cord.
FIGURE 12. A precursor shortly before migration into the ventral cord.
FIGURE 13. A cell death (arrowed) in the p.a.g.
FIGURE 14. L1, showing muscle nuclei beside the gonad.
FIGURE 15. L2 larva of El392 (nuc-1, X), Feulgen stained. The arrows point to persistent DNA from the death of P0c, P1c and P2c. Lateral aspect, magn. x 800.
Web adaptation, Chris Crocker, for Wormatlas, 2008